Evidence map›Paper›PMID 41342252›Full record

ArticleBiology open2025

The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.

Taisuke Sato, Laura L Baxter, April D Adams, Lauren A Bishop, Faycal Guedj, Diana W Bianchi

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In one paragraph

Article in Biology open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Taisuke SatoCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Laura L BaxterCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-7941-1088
April D AdamsCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Lauren A BishopCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Faycal GuedjCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-8847-1119
Diana W BianchiCenter for Precision Health Research, Prenatal Genomics and Therapy Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-9270-5267

Funding

Prenatal Treatment of Down Syndrome to Improve Brain Development and NeurocognitionZIAHG200399 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BIANCHI, DIANA · 2017 to 2025
$11.1M
Intramural NIH HHS ZIA HG200399Japan Society for the Promotion of ScienceNHGRI NIH HHS 1ZIAHG200399NIH HHS
6 · The paper itself

Abstract

Down syndrome (DS) is caused by trisomy for human chromosome 21 (Hsa21) and is associated with atypical neurodevelopment that begins prenatally. The developing human fetus receives nutritional support and gas exchange from the placenta, and normal placental function is essential for proper development. Placentas that sustain fetuses with trisomy 21 contain trisomic cells, but little is known about which Hsa21 genes are overexpressed in the placenta or their downstream molecular, cellular, and functional effects. Although access to human placentas is limited, mouse models of DS provide excellent in vivo systems for investigating the prenatal effects of trisomy. This study examined the placental transcriptome in four mouse models of DS: Dp(16)1/Yey, Ts65Dn, Ts66Yah, and Ts1Cje. Placental gene and protein expression analyses showed that trisomy increased the expression of App, Sod1, and Ifnar1 in Dp(16)1/Yey, Ts65Dn, and Ts66Yah; APP and SOD1 in Dp(16)1/Yey and Ts66Yah; and IFNAR1 in Ts66Yah. Despite modest overlap of trisomy-associated gene dysregulation among these four models, altered extracellular matrix pathways in all four models and upregulation of immune system pathways in Dp(16)1/Yey and Ts66Yah were identified. Altered redox homeostasis was observed for all four models, with Ts1Cje showing distinct changes in SOD activity and antioxidant capacity in comparison to the other three models. Immunofluorescence staining revealed region-specific upregulation of APP, SOD1, and IFNAR1 in Ts66Yah trisomic placentas. This work provides a foundation for understanding the effects of trisomy for Hsa21 orthologs on the mouse placenta and on prenatal development.

Indexed as

Chromosomes, Human, Pair 21Down SyndromePlacentaTrisomyAnimalsDisease Models, AnimalFemaleGene Expression ProfilingHumansMicePregnancyTranscriptomeDown syndromeMouse modelsTranscriptomicsTrisomy 21

Identifiers

PMID41342252
PMCPMC12755066

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